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Adherence of synovial cells on EDA‐containing fibronectin
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AbstractObjective. To investigate the role of EDA‐containing fibronectin (EDA+ FN), a splice variant of FN detectable in association with cellular transformation, in the adherence of synovial cells (SC) on rheumatoid cartilage surface.Methods. The number of SC adherent on cartilage slices or on culture plates containing either EDA+ FN or plasma FN (pFN) was enumerated under a phase‐contrast microscope. The portion of the FN molecule responsible for adherence of SC onto EDA+ FN was investigated by inhibition studies using antibodies or peptide fragments.Results. SC adhered more strongly on the surfaces containing EDA+ FN than on those containing pFN (P < 0.01). When monoclonal antibodies against the EDA or the carboxyl‐terminal heparin‐binding (Hep2) domains were used, adhesion of SC onto EDA+ FN was reduced to a level comparable with that onto pFN. FN fragments containing Hep2 or heparan sulfate inhibited the adhesion of SC onto EDA+ FN. Treatment of SC with heparitinase, but not heparinase, reduced the adhesion of SC onto EDA+ FN.Conclusion. EDA+ FN enhances adherence of SC on the matrix via the Hep2 region of EDA+ FN.
Title: Adherence of synovial cells on EDA‐containing fibronectin
Description:
AbstractObjective.
To investigate the role of EDA‐containing fibronectin (EDA+ FN), a splice variant of FN detectable in association with cellular transformation, in the adherence of synovial cells (SC) on rheumatoid cartilage surface.
Methods.
The number of SC adherent on cartilage slices or on culture plates containing either EDA+ FN or plasma FN (pFN) was enumerated under a phase‐contrast microscope.
The portion of the FN molecule responsible for adherence of SC onto EDA+ FN was investigated by inhibition studies using antibodies or peptide fragments.
Results.
SC adhered more strongly on the surfaces containing EDA+ FN than on those containing pFN (P < 0.
01).
When monoclonal antibodies against the EDA or the carboxyl‐terminal heparin‐binding (Hep2) domains were used, adhesion of SC onto EDA+ FN was reduced to a level comparable with that onto pFN.
FN fragments containing Hep2 or heparan sulfate inhibited the adhesion of SC onto EDA+ FN.
Treatment of SC with heparitinase, but not heparinase, reduced the adhesion of SC onto EDA+ FN.
Conclusion.
EDA+ FN enhances adherence of SC on the matrix via the Hep2 region of EDA+ FN.
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